色素上皮衍生因子对植入型凶险性前置胎盘形成的影响及机制研究

Effect of pigment epithelium- derived factor on formation of embedded pernicious placenta previa and mechanism research

目的探讨色素上皮衍生因子(PEDF)对胎盘微血管床形成的影响及其相关的发病机制。方法选择2014年7月-2015年8月福建省立医院产科剖宫产分娩的孕妇32例,其中植入型凶险性前置胎盘患者16例(PA组),另外16例作为对照组。采用免疫组化法检测两组胎盘组织的PEDF及血管内皮生长因子(VEGF)的定位表达,并计数微血管密度(MVD);利用RT-PCR及Western Blot检测胎盘组织中PEDF和VEGF的mRNA和蛋白质表达。利用ELISA法检测孕妇外周血清中PEDF及VEGF水平。结果 1两组胎盘PEDF及VEGF主要表达在胎盘血管内皮细胞上。PEDF及VEGF的mRNA和蛋白含量差异均有统计学意义(P<0.05)。2两组胎盘MVD含量差异均有统计学意义(P<0.05)。3两组外周血中PEDF水平差异无统计学意义(P>0.05)。结论植入型凶险性前置胎盘组织低表达PEDF,与VEGF及MVD均呈负相关关系,说明植入型胎盘组织PEDF的表达过低是导致对VEGF抑制不足及胎盘病理性血管形成的原因。

Objective To explore the effect of pigment epithelium-derived factor （PEDF） on formation of placental microvascular bed and related mechanism. Methods From July 2014 to August 2015, 32 pregnant women receiving cesarean section in the hospital were selected and divided into embedded pernicious placenta previa group （observation group） and control group, 16 women in each group. The locations and expressions of placental PEDF and vascular endothelial growth factor （VEGF） in the two groups were detected by immunohisto- chemistry. Mierovessel density （MVD） was counted. RT-PCR and Western Blot were used to detect the expressions of PEDF and VEGF mRNA and proteins in placental tissues. ELISA was used to detect the levels of serum PEDF and VEGF in peripheral blood. Results In the two groups, PEDF and VEGF mainly located in endothelial cells of placenta. There were statistically significant differences in the expressions of PEDF and VEGF mRNA and proteins between the two groups （ P〈0. 05 ） . There was statistically significant difference in placental MVD between the two groups （ P〈0. 05 ） . There was no statistically significant difference in PEDF level in peripheral blood between the two groups （ P〉0.05 ） . Conclusion Low expression of PEDF in placenta of patients with embedded pernicious placenta previa is negatively correlated with VEGF and MVD, which indicates that the low expression of, PEDF in placenta tissue is a reason of insufficient inhibition on VEGF and placental pathological neovascularization.